Researchers at Edinburgh University have published two reports on their findings regarding the role of cholesterol production in the body’s virus-suppression response; and fatigue expert Jacob Teitelbaum has a theory as to how this new understanding may play into therapies for 'chronic fatigue syndrome' (ME/CFS) and fibromyalgia.

Study #1: Mar 2011

In March 2011, researchers at Edinburgh University led by Steven Watterson and Prof. Peter Ghazal reported finding that the body fights viral infection by suppressing cholesterol production.(1)

That is, they found that “a key immune hormone stimulated upon infection can lower cholesterol levels and thereby deprive viral infections of the sustenance they need to grow.”

A finding suggesting that, with further research, it might be possible to mimic or encourage these immune signals so as to:

• Bolster the body’s response to viral infection as an alternative to antiviral therapies that attack the virus itself.

• And/or lower cholesterol naturally, as an alternative to use of statin drugs, and potentially without the statin drugs’ often harmful collateral damage to muscle and other cells.

At that time, fatigue and nutrition specialist Jacob Teitelbaum, MD, proposed a theory regarding how this discovery might offer some answers for treatment of ‘chronic fatigue syndrome’ (ME/CFS).

A long-time critic of statin drug over-use, Dr. Teitelbaum begins: “New research suggests that statins might have a very helpful antiviral effect at high dose, and they may even hold promise as an effective new therapy for CFS and fibromyalgia if special (and simple) precautions are added in. The new theory I will present today also offers new possibilities for helpful and easy testing and therapy, while offering an understanding of a large new piece of the CFS/FMS puzzle.” See “Statins, Coenzyme Q10, and Pregnenolone for Addressing CFS” at www.vitality101.com.

Study #2: Sep 2012

Now the Edinburgh team has published a second study that explains the body’s cholesterol-related viral response more specifically – suggesting even more promising therapeutic possibilities for cholesterol controlling and anti-viral therapies.(2)

What they find is that this innate viral response mechanism appears to avoid the collateral damage of statin drugs. As they point out, “high levels of cholesterol increase the risk of heart disease but, because cholesterol is vital to ensure the body’s normal function, managing levels in the blood can be difficult.”

• Statin drugs curb cholesterol production - a complex series of chemical reactions that take place in the liver - by blocking the entire process at one specific point upstream.

• However, because statin drugs do block this entire cascade of reactions, they prevent the production of other molecules that play crucial roles in the body, such as making cell & mitochondrial membranes, and production of hormones, vitamin D, etc.

• By comparison, rather than blocking all these chemical reactions at one point in the cascade, the body’s natural means of suppressing cholesterol to defend against viruses simply slows every step, enabling the other essential functions to continue.

Remember, statins do more than decrease cholesterol, a vital, essential substance especially in the brain and myelin.
Cholesterol--Making or Breaking the Synapse
Ben A. Barres and Stephen J. Smith
Synapses are regions where neurons meet and communicate. But how is their formation regulated in the developing and adult brain? As Smith and Barres explain in their Perspective, the answer could not be simpler. It turns out that, at least in the culture dish, a type of glial cell called an astrocyte produces the molecule cholesterol, which is taken up by neurons and then directs formation of synapses perhaps by regulating vital signaling pathways (Mauch et al.).

Neurons need cholesterol secreted by glial cells to form and maintain functional synapses. And cholesterol is necessary for synaptogenesis and probably for production and transport of vesicles necessary for neurotransmission. If one accepts the concept of neuronal plasticity in the adult brain, then deliberately suppressing cholesterol metabolism in the brain seems questionable.
Excerpted from an article available online:
Steven K Baker MD and Mark A. Tarnoplasky, MD PhD. Statin myopathies: phathophysiologic and clinical perspectives. Clin Invest Med 2001; 24(5): 258-72

Cholesterol biosynthesis and the isoprenoids:
The inhibition of HMG-CoA reductase by the HMGRIs
is approximately 14 steps and 9 to 10 enzymatic
reactions removed from the terminal step(s) in cholesterologenesis
Furthermore,
mevalonic acid, the immediate product of HMG-CoA
reductase, is a pivotal precursor intermediate which
gives rise to the vital isoprenoids en route to cholesterol.
It is not surprising, therefore, that inhibiting this
important biosynthetic pathway causes pleiotropic
metabolic consequences33,34 (Fig. 1).
Prenylation is a fundamental element of posttranscriptional
lipid modification of proteins and other
compounds and affects their function. Some of the
known isoprenoids include the following: (1)
isopentyladenosine, required for transfer RNA synthesis;
(2) dolichols, required for glycoprotein synthesis;
(3) heme A, a polyisoprenoid component of the electron
transport chain; and (4) ubiquinone, a polyisoprenylated
quinoid cofactor of the electron transport
chain, which accepts electrons from complexes I and
II.6,35,… It is estimated that
over 1% of mammalian cellular proteins are isoprenylated.
38 Isoprenylated proteins have been implicated in
smooth muscle cell migration and proliferation,33 and
skeletal muscle cell growth and differentiation.39–42
These conclusions were borne out of experiments in
which statin treatment impaired cell development in
culture, whereas the coapplication of mevalonate or
its distal metabolites (i.e., farnesol or geranylgeraniol)
reversed many of the inhibitory cellular effects of
statins.

in reference to #1--interference with tRNA--statins interfere with selenoprotein tRNA, and specifically decrease selenoprotein N. the glutathione peroxidase family, and the thioredoxin reductases, were recently identified as selenoproteins. theoretically, thru this action, statins could interfere with glutathione reductase activity which re-cycles glutathione within the brain--the major anti-oxidant within the brain.

in reference to #2--dolichols--the substantia nigra is composed largely of lipids. the Most abundant lipid comprising the Substantia Nigra is DOLICHOLS- accounting for up to 45% of the total amt of lipids within this structure.

# 3--decreasing heme A--recent evidence that reduced heme A is a pathologic finding in alzheimer's

#4 decreases CoQ10--literature is filled with the important role of CoQ10 and mitochondrial function esp production of ATP. Seems counterintuitive to depress this vital cofactor in individuals whose mitochondria are dysfunctional already!

statins also interfere with the funciton of lipid rafts --important functions of lipid rafts in refererence ot neuro system:

excerpted from "Membrane Lipid Rafts and their role in Axon Guidance. Guirland, C and Zheng, J Q.

"...Lipid rafts have recently received considerable attention because they are thought to be involved in many cellular functions, in particular, signal transduction for extracellular stimuli. Many of these functions
are also intimately related to the processes involved in neural development, including neurotrophic factor signaling and synaptic plasticity. Recent studies from our lab and others have indicated an important role for lipid rafts in axonal growth and guidance. Specifically, our data show that lipid rafts on the plasma membrane provide platforms for spatial and temporal
control of guidance signaling by extracellular cues..."
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One puzzling finding when I was evaluated by many top specialists for CFS was extremely low cholesterol, in the bottom 5% of the population. It was so low it seemed to cause consternation among the endocrinologists. They seemed puzzled to me. They told me I must have genetically low cholesterol. I do not think my pregnelone was tested.

At the time, I had just been recovering from 5 serious infections for 13 months. These included two viruses (CMV, EBV), two pneumonias (chlamydia pneumonia, mycoplasma pneumonia), and systemic candida (PCR blood test). Interestingly, chlamydia pneumonia is hard to treat because it hides within cells, so does this interferon reaction also occur with intracellular bacteria?

I lost virtually all of my testosterone production (I'm a woman), and have had it supplemented for years. Although I recovered and had normal levels of other hormones, my testosterone never returned to normal.

I have tried CoQ10 supplementation, but find I am very, very sensitive to it. With very small doses (smallest I can find over the counter), my heart races when I take it. Could this be due to the body adjusting to low levels?

I also had hypothyroid problems, but these appear to be secondary to adrenal problems and low testosterone.

As part of my recovery, I went on the fat/protein metabolic type of eating (see William Walcott, Metabolic Typing). This included putting much cholesterol back into my food. I started once again eating butter, cream, red meat, etc. and over about a month, I could feel the strength returning to my body.

So, all in all, I would say that my experience (documented by extensive clinical lab testing) was consistent with this observation. What an insight! And it should be noted, that I had this experience, and I recovered from CFS and have full functionality.

Does this mean that now that I am recovered with low/dormant viral counts, I should once again watch my cholesterol?